MOLECULAR DIVERSITY
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2026
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IF 4.3
Deng Yasi,Liang Ling,Lin Haokai,Shen Xinyang,Zheng Hao,Deng Ying,Tian Xing,Huang Juan,Zhang Ye,Li Bin,Yu Huanghe,Wang Wei
Eucommiae Folium (EF) is a dual-purpose substance utilized in both medicine and nutrition, commonly incorporated into porridge and tea. Traditionally, it is recognized for its ability to tonify the kidney and liver, strengthen muscles and bones, lower blood pressure, and exhibit anti-aging effects. This study aims to investigate the primary components and mechanisms underlying the anti-rheumatoid arthritis (RA) properties of aqueous extract of EF. To identify the material basis of aqueous extract of EF, we employed liquid chromatography-mass spectrometry (LC-Orbitrap-MS) for component analysis using database software. Subsequently, a network approach was applied to pinpoint key anti-RA targets and pathways in order to validate its potential as an effective anti-RA agent. An adjuvant-induced arthritis (AIA) rat model was established, with oral administration of aqueous extract of EF over 30 consecutive days to evaluate its therapeutic effects. The results indicated that LC-Orbitrap-MS identified 29 principal compounds, including geniposidic acid, asperuloside, chlorogenic acid, kaempferol, aucubin, and trifolin. Pharmacological network analysis suggested that these components may exert their therapeutic effects on RA through modulation of NF-κB and PI3K-AKT signaling pathways. Furthermore, oral administration significantly reduced paw swelling in AIA rats while histological analysis demonstrated suppression of inflammatory responses in paw tissues by inhibiting NF-κB and PI3K-AKT pathways.
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS
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2026
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IF 5.4
Chuanju Wang,Qiang Peng,Qianhua Zhang,Shihua Han,Lingyong Zeng,Jiarong Su,Guixin Liang,Zihao Chen,Juan Guo,Yongguang Bi,YuShi Gong,Shaofan Tan,Huaicheng Qin
Pithecellobium clypearia Benth polyphenols (PCBPL) possess potent antioxidant and anti-inflammatory properties, making them promising agents for ulcerative colitis (UC) therapy. However, their clinical translation is hindered by poor water solubility, low stability, and limited bioavailability. To overcome these limitations, Pithecellobium clypearia Benth polyphenols liposomes (PCBPL-Lips) were prepared via thin-film hydration. The resulting PCBPL-Lips exhibited a high encapsulation efficiency of 89.31 ± 1.09%, an average particle size of 124.51 ± 7.61 nm, and a zeta potential of −31.62 ± 2.37 mV. Transmission electron microscopy confirmed their uniform particle distribution, spherical morphology, and smooth surfaces. Stability evaluations showed that PCBPL-Lips remained stable under various pH, temperature, and ionic strength conditions. In vitro digestion studies revealed a sustained-release profile, suggesting potential for prolonged therapeutic action. Biocompatibility assessments showed a hemolysis rate below 5% and cell viability above 80%, indicating excellent safety. In vitro activity assays demonstrated that liposomal encapsulation preserved the antioxidant activity of PCBPL and significantly enhanced its anti-inflammatory efficacy. In a murine model of UC, PCBPL-Lips alleviated clinical symptoms, reduced body weight loss, increased colon length, decreased spleen index and tumor necrosis factor-alpha (TNF-α) levels, and improved colonic tissue architecture. This study demonstrates that liposomal encapsulation markedly enhances the stability, bioavailability, and therapeutic efficacy of PCBPL, providing a promising strategy for its use in the treatment of inflammatory bowel diseases.
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JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Han Zhiqiang,Chen Qiao,Duan Xinmei,He Zhigui,Mou Nianlian,Cao Yu,Ou Yangsipei,He Houhua,Zhang Can,Yang Xu,Qu Kai,Zhang Kun,Malashicheva Anna,Zhong Yuan,Li Chuanwei,Fu Li,Wang Guixue,Wu Wei
Atherosclerotic plaques are characterized by oxidative stress and inflammatory responses, which amplify each other in a vicious cycle, leading to progressive plaque destabilization and ultimately serious cardiovascular events. Therefore, the development of nanoformulations with synergistically enhanced anti-inflammatory and antioxidant activities and effective aggregation in plaques is ideal. In this study, we prepared a gallic acid (GA)-cerium metal polyphenol nanoconjugate (GA-Ce, GC) through cerium ions-mediated oxidative coupling of GA, followed by functionalization of its surface with a phosphatidylserine (PS)-binding peptide (GC-PS, GCP), and subsequent encapsulation with a P-selectin glycoprotein ligand-1 (PSGL-1)-overexpressing endothelial cell membrane (PEM) to harvest a biomimetic PEM@GCP nanozyme. The in vitro results showed that PEM@GCP could effectively scavenge free radicals, promote macrophage differentiation to the M2 phenotype, reduce the content of proinflammatory cytokines, inhibit lipid peroxidation, and inhibit apoptosis with cytoprotective functions. In the atherosclerotic mouse model, compared with the control, PSGL-1-based PEM@GCP resulted in a 4.04-fold greater accumulation in plaque lesions. Through its synergistic anti-inflammatory and antioxidant activities, it effectively blocks the vicious cycle of inflammation-oxidative stress, thereby significantly ameliorating the pathological microenvironment and leading to a substantial 71.3% reduction in the plaque area. These studies elucidate the therapeutic potential of a biomimetic metal-polyphenol nanozyme in the treatment of atherosclerosis, demonstrating its potential as a promising candidate for clinical translation. Graphical
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ANALYTICAL CHEMISTRY
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2026
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IF 7.3
Qingfei He,Lingjun Cheng,Yuanyuan Yang,Zhiyan Zou,Canping Su,Xuan Shi,Jiaming Chen,Weirong Huang,Zhenyu Lin,Guolin Hong
Gold nanoclusters (AuNCs) are emerging electrochemiluminescence (ECL) emitters with unique luminescence and high stability. However, conventional AuNC-based ECL systems, which rely on single-signal regulation, often exhibit weak signal responses and limited stability. To address the challenge of detecting extremely low concentrations of the Alzheimer’s disease (AD) blood biomarker Aβ40, this study presents a novel ECL-based biosensing platform that leverages dual-signal regulation of AuNCs via glutathione (GSH) and H2O2 serving as ECL quenchers. Based on the peroxidase-like activity of the Aβ40–hemin complex, this system restores the ECL signal by catalyzing the consumption reaction between GSH and H2O2. Using this mechanism, a dual-regulation ECL platform was developed, demonstrating a linear detection range of 0.001–100 ng/mL for Aβ40 with a detection limit of 0.18 pg/mL (S/N = 3). This approach not only offers high sensitivity and specificity but also reduces the complexity of surface modification steps. Overall, this study advances ECL technology through dual regulation and provides a sensitive, practical, efficient, and reliable analytical method for early AD screening.
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JOURNAL OF MOLECULAR STRUCTURE
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2026
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IF 4.9
Xiaoshuang Dai,Na Yao,Xinyu Liu,Ke Mei,Bin Sun,Ziqing Weng,Jianpeng Liu,Junda Liu,Ning Lei,Neng Qiu
Three FA-biotin conjugates were designed with 5-10 × higher cytotoxicity than FA. • These prodrugs self-assembled into nanoparticles, with FS6B forming optimal NPs. • FS6B NPs exhibited excellent stability and dual GSH/pH-responsive drug release. • FS6B NPs showed enhanced biotin receptor-mediated tumor targeting ability. • FS6B NPs exerted anticancer and anti-migration effects with minimal toxicity. Ferulic acid (FA) is widely recognized for its antioxidant and anti-inflammatory properties; however, its potential anticancer activity is limited by poor aqueous solubility and insufficient cellular uptake. In this work, a series of ferulic acid–biotin conjugates containing amino acid linkers of different lengths were synthesized and allowed to self-assemble into nanoparticles (FS4B, FS6B, and FS8B NPs). All nanoparticles had sizes below 200 nm, with FS6B NPs showing the best long-term stability for over 3 months. FS6B NPs exhibited glutathione- and pH-responsive release behavior and demonstrated over 10-fold stronger cytotoxicity toward 4T1 cells compared with free FA. Biotin-mediated cellular uptake was improved, accompanied by increased apoptosis induction. Furthermore, FS6B NPs significantly inhibited 4T1 cell migration, with a migration rate of 54.47%, in comparison with 72.51% for FA and 85.60% for the control. Meanwhile, FS6B NPs showed negligible toxicity toward normal cells and no detectable hemolytic activity. These results demonstrate that self-assembled FA-biotin nanoprodrugs possess favorable physicochemical properties and in vitro biological activity, providing insight into the structural modification and functional application of FA-based nanomaterials.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
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IF 8.7
Yajuan Chen,Yifan Ouyang,Mingkang Yang,Niuniu Zhang,Pengqian Zhou,Jinjing Xu,Yan Chen,Jiwei Wang
The injectable hydrogel with self-healing and strong adhesive properties was developed. • Carbon dots derived from Isatis root were synthesized and loaded into the hydrogel. • The hydrogel exhibits pH/ROS-responsive drug release behavior. • The hydrogel exhibits antibacterial activity, antioxidative capability • The hydrogel accelerates infected wound healing. Bacteria-infected wounds are very difficult to treat, largely because the pathological microenvironment involved is dynamic. The requirements for infected wound repair are multifaceted, and conventional hydrogel dressings cannot adequately meet them due to their limited functionality. In this study, we report the construction of a multifunctional, pH/ROS dual-responsive hydrogel based on dynamic Schiff base and borate ester linkages. Oxidized pullulan (OPu) was used to fabricate the hydrogel, and the bioactive polyphenol chlorogenic acid (CA) acted as the crosslinking agent. Next, we synthesized the carbon dots derived from Isatis root (IR-CDs) using the hydrothermal method and subsequently incorporated them into the hydrogel. The hydrogel exhibited excellent injectability and self-healing capability, enabling application at irregular wound sites. Under the acidic and oxidative conditions of infected wounds, the hydrogel gradually dissociated, releasing IR-CDs and CA in a controlled manner. IR-CDs exhibited potent antibacterial activity, while CA and IR-CDs in combination efficiently scavenged excessive reactive oxygen and nitrogen species, therefore promoting tissue regeneration and reducing inflammation. Both in vitro and in vivo evaluations confirmed that the hydrogel was highly biocompatible and provided anti-infective, anti-oxidative, and anti-inflammatory effects during the early stages of healing, followed by an increase in angiogenesis and acceleration of the wound healing process. The hydrogel developed in this study is versatile and can serve as a promising and effective biomaterial platform for managing bacteria-infected wounds.
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Drug Design Development and Therapy
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2026
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IF 6.1
Dong Fan,Zongming Wang,Shixue Luo,Xuanhao Huang,Xingyi Yuan,Yanan Wang,Zhongyu Wang,Huitong Chen,Weiwen Wang,Yuxin Ma,Chang Zhou,Xiaobao Jin,Jing Liu,Xin Wang
Background: Nonfunctioning pituitary adenoma (NFPA) is among the most prevalent intracranial tumors. As surgical resection remains the primary treatment, there is a need for new therapeutic strategies. Plumbagin (PLB), a bioactive naphthoquinone compound derived from the roots of Plumbaginaceae Juss, has been used in anti-tumor research in recent years, but its mechanism remains controversial.Purpose: The aim of this study was to explore the molecular mechanism of PLB-induced ferroptosis in NFPA.Methods: The cell viability of PLB against PDFS cells was first assessed by CCK-8, colony formation, and EDU assays. Network pharmacology, molecular docking, and molecular dynamics were then used to screen out targets associated with ferroptosis. Finally, the Nrf2/FTH1 pathway was validated by a 3D multicellular tumour spheroids (MCTSs) model, q-PCR, and Western blot in vitro and in vivo.Results: Compared to temozolomide (TMZ), PLB more potently inhibited the viability of PDFS cells. In vitro, PLB treatment was associated with downregulation of the Nrf2/FTH1 pathway, accompanied by increased lipid peroxidation and labile iron pool (LIP) accumulation. Furthermore, PLB treatment led to the upregulation of NCOA4 and an increase in intracellular free iron, consistent with ferritinophagy activation. These effects collectively point to the induction of ferroptosis.Conclusion: This study demonstrates that PLB may induce ferroptosis in PDFS cells. The mechanism involves suppression of the Nrf2/FTH1 pathway, subsequent upregulation of NCOA4, and ferritinophagy-driven iron overload. These results identify PLB as a potential ferroptosis inducer and warrant further investigation into its therapeutic potential for NFPA. The image shows a biochemical pathway illustrating ferritinophagy and ferroptosis. Iron in the form of Fe superscript 3 is transported by transferrin into the cell, where it is stored in ferritin. Ferritin is directed to the autolysosome, facilitated by Lamp2, where iron is released as Fe superscript 2. NCOA4 and LC3 are involved in ferritinophagy, leading to the labile iron pool. The Fenton reaction produces reactive oxygen species, contributing to ferroptosis. Nrf2 regulates FTH1, with arrows indicating promotion and inhibition. Plumbagin is shown affecting the pathway, with an illustration of a mouse receiving an injection, highlighting the interaction between NCOA4, FTH1 and Nrf2 in the brain. Arrows indicate promotion and inhibition effects within the pathway.Diagram of ferritinophagy and ferroptosis: iron regulation, NCOA4, FTH1, Nrf2 and plumbagin effects.
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FOOD HYDROCOLLOIDS
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2026
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IF 13.8
Rui Hu,Da-Wen Sun,Liang Xu,Tingting Gao,You Tian
Preserving biological functionality under cryogenic conditions remains essential across biotechnology, food, and healthcare sectors, yet conventional cryoprotectants such as dimethyl sulfoxide (DMSO) and glycerol pose significant cytotoxic and environmental concerns. Herein, a sustainable cryopreservation strategy based on hydrocolloid-like micro eutecto-vesicles (MEVs), fabricated via a facile centrifugal process using glucose/fructose (GF), proline/glucose (PG), and proline/sorbitol (PS) based natural deep eutectic solvents (NADESs), and sodium alginate (SA), was developed, which was dual bioinspired by cold-tolerant organisms and frog eggs. The results showed that the introduction of NADESs can improve the colloidal stability and uniformity of the MEVs preparation process, and the diameter of the MEVs obtained at 1000 rpm centrifugal speed was about 300 μm. The toxicity test for yeast showed that the components used were less toxic than glycerol and DMSO in terms of proliferation activity and ROS accumulation. For the evaluation of post-thaw cell viability, the cryoprotection of SA/PG based MEVs can achieve a survival rate of yeast cells higher than 92%, while ensuring the integrity of cell structure and excellent proliferation activity. The subsequent mechanism exploration showed that the colloidal vesicle structure of MEVs can reduce the formation of intercellular ice crystals during freezing and inhibit the recrystallization of ice crystals. This study presents a biocompatible, scalable, environmentally responsible, and food grade hydrocolloid-based platform for the long-term stabilization of biological systems, with direct implications for sustainable probiotic production, cold-chain logistics, and bioresource preservation.
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TISSUE & CELL
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2026
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IF 3.1
Chen Chen,Qin Yu,Chen Xi,Minjuan Xie,Yinjie Jiang,Jie Zhou
Norcantharidin (NCTD) induces nephrotoxicity via mitochondria-dependent apoptosis. • The nephrotoxicity of NCTD involves inhibition of the ATF4/CTH/H 2 S pathway. • NCTD suppresses ATF4-driven CTH expression, reducing H 2 S production. • NCTD reduces H 2 S, impairing Drp1 S-sulfhydration and mitochondrial function. • ATF4, CTH, and H 2 S are potential therapeutic targets for NCTD-induced kidney injury. Norcantharidin serves as a therapeutic agent in the clinical care of malignant neoplasms. However, recent safety alerts issued in China in June 2025 highlighted its association with renal injury. Given that the mechanisms underlying NCTD-induced nephrotoxicity have yet to be completely defined, this work was designed to explore the impact of the ATF4/CTH/H 2 S pathway on nephrotoxicity triggered by NCTD. Our data revealed that exposure to NCTD triggered mitochondria-dependent apoptosis in renal cells, alongside decreased H 2 S levels, ROS accumulation, compromised mitochondrial integrity, and caspase-3 activation. Mechanistically, NCTD inhibited both ATF4 protein levels and its transcriptional function, resulting in downregulation of CTH and a subsequent reduction in H 2 S production. H 2 S deficiency impaired S-sulfhydration of Drp1, enhanced the Drp1-VDAC1 interaction, promoted mPTP opening, and ultimately triggered apoptosis. H 2 S supplementation rescued these defects by restoring Drp1 S-sulfhydration, but this protective effect was completely abolished by DTT, confirming the specificity of S-sulfhydration. Furthermore, overexpression of ATF4 or CTH alleviated NCTD-triggered apoptosis via H 2 S restoration, whereas knockdown of ATF4 or CTH exacerbated cytotoxicity. Critically, CTH knockdown abolished the protective effect of ATF4 overexpression, while CTH overexpression remained functional independently of ATF4. In conclusion, our findings established that NCTD induced nephrotoxicity primarily through the inhibition of the ATF4/CTH/H 2 S axis, which disrupted Drp1-mediated mitochondrial homeostasis. These results identified H 2 S restoration as a promising therapeutic strategy to mitigate NCTD-induced kidney injury.
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SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
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2026
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IF 4.8
Qin Xiong,Tiansheng Zhao,Yuyan Liu,Xin Sui,Yanlan Xu,Cheng Wang,Fanglan Liu,Chunhua Xia,Na Li
Accurate discrimination of structurally similar antibiotics remains a major challenge due to the limited resolving capability of conventional sensing signals. Tetracycline antibiotics, which often coexist in complex matrices, typically generate highly overlapping responses, hindering reliable identification. Herein, a dual-emission fluorescence sensing platform based on Eu 3+ -functionalized silver nanoclusters (AgNCs@Eu 3+ ) was developed to generate analyte-dependent signal patterns. Upon interaction with tetracyclines, the green emission of AgNCs is selectively attenuated through the inner filter effect, while the coordination between tetracyclines and Eu 3+ activates a characteristic red emission by the antenna effect. The synergistic modulation of these two signals produces partially overlapping but distinguishable fluorescence fingerprints for different tetracycline species. To resolve these subtle differences, machine learning algorithms were employed to decode the dual-channel fluorescence responses. The optimized model enables accurate classification of tetracycline, oxytetracycline, doxycycline, and chlortetracycline, with an accuracy up to 0.99. The platform further demonstrates robust performance in pharmaceutical, milk, and environmental water samples, maintaining reliable discrimination despite matrix interference. This work establishes a strategy that couples mechanism-defined dual-emission sensing with data-driven analysis, providing a practical route for the identification of structurally similar analytes in complex systems.
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ANALYTICAL CHEMISTRY
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2026
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IF 7.3
Tao Ma,Chenxing Xu,Siyuan Li,Siqi Hu,Kaizhi Ding,Jinpeng Yu,Pengcheng Wei,Dongting Zhangsun,Xiaopeng Zhu,Sulan Luo
α6β4 nicotinic acetylcholine receptors (nAChRs) represent potential therapeutic targets for pain management; however, studies on the distribution and function of these receptors have been constrained by the scarcity of pharmacological tools. An analogue of α-conotoxin (α-CTx) LvIC from Conus lividus, [D1G, Δ14Q]LvIC, selectively inhibits heterologous rat α6/α3β4 nAChRs (where α6/α3 denotes the chimeric subunit) and represents a promising pharmacological tool. However, its limited stability may restrict further applications. Rational design based on the [D1G, Δ14Q]LvIC analogue led to the identification of a key mutant, [d-Lys11]LvIC, with a half-maximal inhibitory concentration (IC50) of 8.2 nM. The mutant retained the desired activity and substantial selectivity for 11 other nAChR subtypes while demonstrating superior stability in rat serum. Based on these favorable properties, we conjugated the analogue to a BODIPY-FL (BDP) fluorophore to obtain a high-fidelity fluorescent probe, enabling the investigation of α6β4 nAChRs tissue distribution in rats. The fluorescent probe, [d-Lys11]LvIC-BDP, was preliminarily applied to detect a reduction in α6β4 nAChRs expression in a cyclophosphamide (CYP)-induced rat model of interstitial cystitis/bladder pain syndrome (IC/BPS). The development of this fluorescent probe provides an ideal tool for investigating the tissue distribution and functional characterization of α6β4 nAChRs.
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ADVANCED FUNCTIONAL MATERIALS
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2026
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IF 19.9
Yuping Jiang,Fenglan Zhang,Junyao Song,Yi Dai,Yingshan Qu,Zhenzhen Zhu,Wenhua Xu,Jinsheng Shi,Xiaoying Kong
Metformin (Met) is recognized as a star drug with multi-pathway anti-cancer potential, yet conventional Met-based therapies remain limited by insufficient targeting and failure to reverse adaptive metabolic reprogramming. Triple-negative breast cancer (TNBC) cells develop Met resistance via dysregulated mitochondrial oxidative phosphorylation (OXPHOS) and metabolic flexibility. Herein, we present a mitochondrial metabolic reprogramming strategy that fully exploits the dependence of TNBC cells on OXPHOS to induce selective biological energy collapse. A mitochondria-targeted multifunctional nanoplatform (M@AMT NPs) was constructed via integrating ammonia borane (AB), Met, and triphenylphosphine (TPP) onto molybdenum disulfide (MoS 2 ) nanoflowers. M@AMT NPs equipped with pH/NIR-responsive modules enables synchronized hydrogen-photothermal-chemodynamic therapy. TPP moiety enables precise mitochondrial localization, triggering a self-amplifying therapeutic cycle wherein local hydrogen/photothermal/chemodynamic perturbation-induced mitochondrial dysfunction abrogates OXPHOS and consequently exacerbates subsequent metabolic catastrophe. Mitochondria-localized H 2 synergizes with Met to disrupt ATP production, downregulate heat shock proteins, and restore Met sensitivity. In contrast to conventional resistance-reversing interventions, this approach exploits the intrinsic metabolic adaptability of resistant cancer cells to provoke self-driven collapse. This work establishes a new class of metabolically adaptive nanomaterials capable of reprogramming mitochondrial energy metabolism, offering a versatile platform for precision therapy against Met-resistant TNBC.
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